Spinal Cord Injury Induced c-fos Expression is Reduced by p-CPA, a Serotonin Synthesis Inhibitor. An Experimental Study
Influence of serotonin on upregulation of cellular-fos (c-fos) following a focal spinal cord injury was examined using immunohistochemistry in a rat model. Spinal cord injury was produced by making a unilateral longitudinal incision of the dorsal horn of
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Spinal Cord Injury Induced c-fos Expression is Reduced by p-CPA, a Serotonin Synthesis Inhibitor. An Experimental Study Using Immunohistochemistry in the Rat H. S. Sharma l , J. Westman!, T. Gordh 3 , and F. Nyberg2 1 Laboratory
of Neuroanatomy, Department of Medical Cell Biology, Department of Pharmaceutical, Uppsala, Sweden ofPharmacentical Biosciences, Biomedical Centre Uppsala University, Uppsala, Sweden 3 Department of Anaesthesiology, University Hospital, Uppsala University, Uppsala, Sweden 2 Department
Summary Influence of serotonin on upregulation of cellular{os (c{os) following a focal spinal cord injury was examined using immunohistochemistry in a rat model. Spinal cord injury was produced by making a unilateral longitudinal incision of the dorsal hom of the TlO-ll segments. A focal lesion to the cord markedly upregulated c{os immunohistochemistry at 5 h which was mainly located in the edematous regions of the cord in the injured as well as in the perifocal T9 and Tl2 segments. Pretreatment with p-CPA, a serotonin synthesis inhibitor, significantly attenuated the c{os upregulation along with the edematous expansion of the cord. These results for the first time suggest that trauma induced release of serotonin and edema formation are important biological signals inducing c{os expression.
Keywords: Spinal cord injury; c-fos immunohistochemistry; p-CPA; spinal cord edema.
Introduction Spinal cord injury is a serious clinical problem. Depending upon the magnitude and severity of the initial impact, spinal trauma will lead to life time disability of the victims involving huge amount of financial burden on the society [9, "15, 16]. Thus every efforts should be made to minimise the consequences of spinal injury in order to preserve the integrity and function of the spinal cord. One way to understand this problem is to identify series of events that are taking place in early phase of spinal cord trauma. This would expand our knowledge regarding the mechanisms of spinal cord dysfunction following trauma. There are reports indicating that events occurring within 8 h periods following primary insult will set the stage for the later spinal cord dysfunction leading to
permanent disability [3, 9, 16]. Thus suitable pharmacological therapy if introduced within 8 h time window after insult will have some beneficial effects on the recovery of spinal cord function in patients. Any therapy given after 8 h primary insult is simply ineffective [9, 16). Thus, further studies should be carried out in greater details to understand the basic early events following trauma. This would help to explore probable therapeutic measures to minimise spinal cord dysfunction leading to permanent disability. Our laboratory is engaged since the last 13 years to understand the basic mechanisms of early cell reactions following trauma in a rat model [10, 11, 16). Our observations show that trauma to the spinal cord upregulates several cellular proteins and enzymes such as heat shock protein (HSP 72 kD), glial fibrillary acidic protein (GFAP),
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